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Current risk allocation schemas are imperfect, as some children are classified as lower\u2010risk and treated with less intensive therapy relapse, while others deemed higher\u2010risk are probably over\u2010treated. Most cooperative groups previously used morphological clearance of blasts in blood and marrow during the initial phases of chemotherapy as a primary factor for risk group allocation; however, this has largely been replaced by the detection of minimal residual disease (\n                    <jats:styled-content style=\"fixed-case\">MRD<\/jats:styled-content>\n                    ). Other than age and white blood cell count (\n                    <jats:styled-content style=\"fixed-case\">WBC<\/jats:styled-content>\n                    ) at presentation, many clinical variables previously used for risk group allocation are no longer prognostic, as\n                    <jats:styled-content style=\"fixed-case\">MRD<\/jats:styled-content>\n                    and the presence of sentinel genetic lesions are more reliable at predicting outcome. Currently, a number of sentinel genetic lesions are used by most cooperative groups for risk stratification; however, in the near future patients will probably be risk\u2010stratified using genomic signatures and clustering algorithms, rather than individual genetic alterations. This review will describe the clinical, biological, and response\u2010based features known to predict relapse risk in childhood\n                    <jats:styled-content style=\"fixed-case\">ALL<\/jats:styled-content>\n                    , including those currently used and those likely to be used in the near future to risk\u2010stratify therapy.\n                  <\/jats:p>","DOI":"10.1111\/bjh.12442","type":"journal-article","created":{"date-parts":[[2013,6,29]],"date-time":"2013-06-29T03:24:47Z","timestamp":1372476287000},"page":"606-620","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":94,"title":["Predicting relapse risk in childhood acute lymphoblastic leukaemia"],"prefix":"10.1111","volume":"162","author":[{"given":"David T.","family":"Teachey","sequence":"first","affiliation":[{"name":"Pediatric Hematology and Oncology Children's Hospital of Philadelphia University of Pennsylvania School of Medicine Philadelphia PA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen P.","family":"Hunger","sequence":"additional","affiliation":[{"name":"Pediatric Hematology\/Oncology\/BMT University of Colorado School of Medicine and Children's Hospital Colorado Aurora CO USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,6,29]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200004063421402"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1200\/JCO.2010.30.1325"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1200\/JCO.2008.16.1117"},{"key":"e_1_2_7_5_1","first-page":"1783","article-title":"Proposals for the immunological classification of acute leukemias. 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